Vasopressin, Angiotensin II and Tyrosine-Hydroxylase Expression in the Hypothalamus of the Syndrome of Inappropriate ADH: A Case Report

Abstract

Abstract:The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a disease characterized by hyponatremia and hyperosmolality of urine, and where vasopressin, angiotensin II and catecholamines are implicated in salt water balance, cardiovascular and blood pressure regulation. Therefore, the aim of this study is to analyze the hypothalamic distribution of vasopressin (VAS) Angiotensin II (AGII) and tyrosine-hydroxylase (TH) in a case of SIADH and compare it with a case without SIADH. Two hypothalamus taken from a 66 year-old man with SIADH, and the other from a 63 year-old man without SIADH, were used. An immunohistochemical study was performed using anti-VAS, anti-AGII and anti-TH as primary antibodies. The vasopressin immunoreactive material was mainly found in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but VAS was also shown in the periventricular nucleus, preoptic medial area, perifornical nucleus and hypothalamic lateral area. The AGII was also mainly found in the SON and PVN. The TH was found in the SON, PVN, arcuate nucleus, periventricular nucleus, perifornical nucleus, preoptic medial and lateral area. VAS was less intensive and in a lesser number of cells and fibres in the case of SIADH, as opposed to the AGII and TH which were similar in both cases.

Angiotensin II, Vasopressin, and Collagen-IV Expression in the Subfornical Organ in a Case of Syndrome of Inappropriate ADH

“…This increase depends on an excessive water intake that overwhelms the restricted renal ability of diluting urine and mounting compensatory diuresis due to vasopressin dysregulation. A previous work [20] showed that vasopressin immunoreactive material was less intensive and was present in a lower number of cells and fibres in the SIADH case where it was mainly found in the whole supraoptic nucleus and the magnocellular part of the paraventricular hypothalamic nucleus. The low intensity of VAS in the case of SIADH could mean an increase in VAS release owing to variations in the vasopressin receptor, since other studies [21] have described cases, whose clinical presentation and laboratory findings were consistent with SIADH but which exhibited unmeasurable VAS levels on repeated occasions that seems to be due to an activating mutation of the vasopressin receptor V2 (V2R).…”